简介:Objective:TumorassociatedantigenencodinggeneHCA520(AF146019)wasidentifiedbyscreeningahumanhepatocellularcarcinomaexpressingcDNAlibraryusingSEREXtechnique.InthisexperimentwestudiedtheeffectofHCA520oncellproliferationandapoptosis.Methods:GeneHCA520wasgainedbyPCRandtransfectedinto293cells.ThestableexpressioncellswereobtainedbyG418selection.Thecellproliferationwasmeasuredby[3H]-TdRuptakeandapoptosisassaywasmeasuredbyFACS.Results:EukaryoticexpressionplasmidpcDNA3-HCA520wasconstructedanditsstabletransfectantswereobtained.OverexpressionofHCA520inhibitedthecellproliferationandenhancedcellapoptosisafterserumdeprivation.Conclusion:HCA520isanoveltumorassociatedantigenthatcanaffectcellproliferationandapoptosis.
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简介:Objective:Weinvestigatedthecorrelationbetweenthenumberofcirculatingtumorcells(CTCs)andwholebodymetabolictumorvolume(WBMTV)measuredby18F-fluorodeoxyglucose(FDG)positronemissiontomography/computedtomography(PET/CT).TheaimwastoevaluatethevalueoftheincorporationofCTCnumberandWBMTVintheprognosticpredictionofstageIIIsmall-celllungcancer(SCLC).Methods:Onehundredandtwenty-ninepatientswereenrolledinthisstudy.Allpatientsweretreatedwithfourcyclesofaplatinum-basedregimenandconcurrentchestirradiation,followedbyprophylacticcranialirradiation.BloodsamplesforCTCanalysiswereobtainedfrom112patientsbeforetheinitiationofchemotherapy(asabaseline),aftercycle1andaftercycle4.CTCsweremeasuredusingtheCELLSEARCH?system.ThepatientsunderwentpretreatmentFDGPET/CTWBMTV,whichincludedallmalignantlesions.TheSpearmanranktestwasusedtodeterminethecorrelationamongCTCcounts,WBMTVanddiseasestage.Overallsurvival(OS)andprogression-freesurvival(PFS)curveswereproducedusingtheKaplan-Meiermethod,andsurvivaldifferencesbetweengroupswereassessedbythelog-ranktest.Results:ThenumberofCTCsatbaselinedidnotcorrelatewithWBMTVbeforetheinitiationoftherapy(P=0.241).ThenumberofCTCsatbaselineandtheWBMTVbeforetheinitiationoftherapywereindependentrelevantfactorsforPFSandOS.Thesubgroupanalysis(GroupA:CTCcount>19.5andaWBMTV>266.5cm^3;GroupB:CTCcount>19.5andaWBMTV≤266.5cm^3;GroupC:CTCcount≤19.5andaWBMTV>266.5cm^3;GroupD:CTCcount≤19.5andaWBMTV≤266.5cm^3)showedthatthedifferenceswerestatisticallysignificantinthemedianPFS(GroupAvs.D,P<0.001;GroupBvs.D,P=0.018;GroupCvs.D,P=0.029)andinthemedianOS(GroupAvs.D,P<0.001;GroupBvs.D,P=0.012).Conclusions:CTCnumberandWBMTVarerelatedtoprogressionanddeathinpatientswithSCLC.TheincorporationofCTCnumberandWBMTVscanscanprovideadetailedprognosticpredictionforSCLC.
简介:AbstractImportance:LIM domain only 1 (LMO1) gene polymorphisms were previously found to be implicated in the risk of several cancers. No available studies were performed regarding the predisposing effect of LMO1 gene single nucleotide polymorphisms (SNPs) on central nervous system (CNS) tumor risk.Objective:We aimed to determine whether the LMO1 gene SNPs were associated with the risk of CNS tumor by applying a case-control study with 191 cases and 248 controls in China.Methods:The contributions of LMO1 gene SNPs to the risk of CNS tumor was evaluated by multinomial logistic regression.Results:Based on the calculations of odds ratio (OR) and 95% confidence interval (CI), we failed to detect a significant relationship between each LMO1 gene SNP (rs110419 A>G, rs4758051 G>A, rs10840002 A>G, rs204938 A>G, and rs2168101 G>T) and CNS tumor risk, respectively. A negative association was also found in the combined effects on these five SNPs and CNS tumor risk. The stratification analysis further demonstrated the individuals with rs204938 AG/GG genotype confer to increased risk of CNS tumor compared with those with an AA genotype in males (OR: 1.74, 95% CI: 1.01-2.98, P = 0.046).Interpretation:We concluded that LMO1 gene SNPs may not strong enough to influence the risk of CNS tumor in Chinese children. More studies are required to verify this association.
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简介:AIM:Toinvestigatethediversecharacteristicsofdifferentpathologicalgradingsofgastricadenocarcinoma(GA)usingtumor-relatedgenes.METHODS:GAtissuesindifferentpathologicalgradingsandnormaltissuesweresubjectedtotissuearrays.Expressionsof15majortumor-relatedgenesweredetectedbyRNAinsituhybridizationalongwith3’terminaldigoxin-labeledanti-sensesinglestrandedoligonucleotideandlockednucleicacidmodifyingprobewithinthetissuearray.Thedataobtainedwereprocessedbysupportvectormachinesbyfourdifferentfeatureselectionmethodstodiscovertherespectivecriticalgene/genesubsetscontributingtotheGAactivitiesofdifferentpathologicalgradings.RESULTS:IncomparisonofpoorlydifferentiatedGAwithnormaltissues,tumor-relatedgeneTP53playsakeyrole,althoughothersixtumor-relatedgenescouldalsoachievetheAreaUnderCurve(AUC)ofthereceiveroperatingcharacteristicindependentlybymorethan80%.ComparingthewelldifferentiatedGAwithnormaltissues,wefoundthat11tumor-relatedgenescouldindependentlyobtaintheAUCbymorethan80%,butonlythegenesubsets,TP53,RBandPTEN,playakeyrole.Onlythegenesubsets,Bcl10,UVRAG,APC,Beclin1,NM23,PTENandRBcoulddistinguishbetweenthepoorlydifferentiatedandwelldifferentiatedGA.Noneofasinglegenecouldobtainavaliddistinction.CONCLUSION:Differentfromthetraditionalpointofview,thewelldifferentiatedcancertissueshavemorealterationsofimportanttumor-relatedgenesthanthepoorlydifferentiatedcancertissues.
简介:interleukin-24(IL-24)能在人的癌症的一个大系列导致apoptosis,是记录得好的MDA-7/IL-24基因的导出的房间线,而是效果在未知的老鼠黑瘤房间遗体上转。IL-24(pEGFP-IL-24)的真核细胞的表示plasmid被DNA再结合技术构造。再结合plasmid和空向量是进B16F0房间的transfected,IL-24的表情被LSM决定,B16F0房间的增长被MTT试金,和apoptosis率测量,B16F0房间的房间周期分发被FCM测量。在老鼠固体肿瘤的IL-24基因transfection的禁止的效果被观察并且测量。与控制相比,B16F0房间的增长被transfection与pEGFP-IL-24禁止,transfected房间的G2/M阶段也是increased.Moreover,在与pEGFP-IL-24与B16F0房间transfected接种以后,有可检测的肿瘤的鼠标的百分比被减少。在老鼠模型的肿瘤的生长率显著地与控制相比在IL-24基因治疗组被禁止。B16F0细胞的增长被pEGFP-IL-24的pEGFP-IL-24transfection.Theintratumor注射禁止能显著地在老鼠禁止稳固的肿瘤的生长。
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简介:AIM:ToinvestigatewhethertheevaluationoftumorbuddingcancomplementK-RASanalysistoimprovetheindividualizedpredictionofresponsetoanti-epidermalgrowthfactorreceptorbasedtherapiesinmetastaticcolorectalcancer(mCRC)patients.METHODS:Forty-threepatientswithmCRCtreatedwithcetuximaborpanitumumabwereenteredintothisstudy.AccordingtotheResponseEvaluationCriteriainSolidTumorscriteria,30patientshadstableorprogressivedisease(non-responsive),while13patientshadapartialresponse.Tumorbudswereevaluatedfromwholetissuesectionsstainedforpan-cytokeratin,evaluatedinthedensestregionusinga40×objectiveand'high-grade'tumorbuddingwasdefinedas15buds/high-powerfield.RESULTS:TumorbudsandK-RASmutationbothcorrectlyclassified68%ofpatients.AllpatientswithK-RASmutation(n=7)orhigh-gradetumorbudding(n=11)werenon-responsive,ofwhich4patientshadbothfeatures.All13partialresponderswereK-RASwild-typewithlow-gradetumorbudding.Combined,thepredictivevalueofK-RASandtumorbuddingwas80%.Additionally,high-gradetumorbuddingwassignificantlyrelatedtoworseprogression-freesurvival[HR(95%CI):2.8(1.3-6.0,P=0.008)].CONCLUSION:Ifconfirmedinlargercohorts,theadditionoftumorbuddingtoK-RASanalysismayrepresentaneffectiveapproachforindividualizedpatientmanagementinthemetastaticsetting.
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简介:Esophagealcancerhasbeenreportedastheninthmostcommonmalignancyandranksasthesixthmostfrequentcauseofdeathworldwide.Esophagealcancertreatmentinvolvessurgery,chemotherapy,radiationtherapy,orcombinationtherapy.Novelstrategiesareneededtoboosttheoncologicoutcome.Recentadvancesinthemolecularbiologyofesophagealcancerhavedocumentedtheroleofgeneticalterationsintumorigenesis.Oncogenesserveapivotalfunctionintumorigenesis.Targetedtherapiesaredirectedattheuniquemolecularsignatureofcancercellsforenhancedefficacywithlowtoxicity.RNAinterference(RNAi)technologyisapowerfultoolforsilencingendogenousorexogenousgenesinmammaliancells.RelatedresultshaveshownthattargetingoncogeneswithsiRNAs,specificallythemRNA,effectivelyreducestumorcellproliferationandinducesapoptoticcelldeath.Thisarticlewillbrieflyreviewstudiesonsilencingtumorenhancergenesrelatedtotheinductionofesophagealcancer.
简介:Theextinctionphenomenoninducedbymultiplicativenon-GaussianL′evynoiseinatumorgrowthmodelwithimmuneresponseisdiscussed.Undertheinfluenceofthestochasticimmunerate,themodelisanalyzedintermsofastochasticdifferentialequationwithmultiplicativenoise.BymeansofthetheoryoftheinfinitesimalgeneratorofHuntprocesses,theescapeprobability,whichisusedtomeasurethenoise-inducedextinctionprobabilityoftumorcells,isexplicitlyexpressedasafunctionofinitialtumorcelldensity,stabilityindexandnoiseintensity.Basedonthenumericalcalculations,itisfoundthatfordifferentinitialdensitiesoftumorcells,noiseparametersplayoppositerolesontheescapeprobability.Theoptimallyselectedvaluesofthemultiplicativenoiseintensityandthestabilityindexarefoundtomaximizetheescapeprobability.
简介:AIM:Toexaminetheassociationofgeneticpolymorphisms(-308)G/ATNFα,(+250)A/GLtα,(+36)A/GTNFR1,(+1663)A/GTNFR2withthedevelopmentofprimaryopenangleglaucoma(POAG)amongpeopleinCentralRussia.METHODS:Thestudysampleincluded443individuals,ofwhich252patientswithPOAGand191individualsinthecontrolgroup.Genotypingof(-308)G/ATNFα,(+250)A/GLtα,(+36)A/GTNFR1,(+1663)A/GTNFR2wasperformedusingpolymerasechainreaction.ThedistributionofallelesandgenotypesofthestudiedDNAmarkersinthegroupswasexaminedby2×2contingencytablesandχ2withtheYates'scorrectionforcontinuityandoddsratios(OR)with95%confidenceintervals(CI).RESULTS:Allele(-308)GTNFα(Р=0.01,OR=1.78,95%CI1.12-2.85)wasidentifiedasariskfactorforPOAG.Homozygotes(-308)AATNFαareatalowestriskfordevelopmentofthedisease(Р=0.01,OR=0.0005).ThefollowingcombinationofgeneticvariantsofcytokineswereassociatedwithareducedriskofPOAG:(+1663)ATNFR2and(+250)GLtα(OR=0.34)CONCLUSION:Geneticpolymorphisms(-308)G/ATNFα,(+250)A/GLtα,(+1663)A/GTNFR2associatedwiththedevelopmentofPOAGinthepopulationofCentralRussia.
简介:Extragonadalprimaryyolksactumoroftheintestinaltractoriginisexceedinglyrare.Throughamultipledisciplinaryteam,thediagnosisandtreatmentofprimaryintestinalyolksactumorwerefurtherdefined.Wereport2suchcaseswithdetailedhistologicandimmunohistochemicalanalysis.Thetwopatientswerea7-year-oldgirlanda29-year-oldwoman.Bothofthempreoperativelyhadanelevatedserumalphafetoprotein(AFP)level(≥1,210ng/mL).Thetumorsarelocatedintheintestineandimagingexaminationindicatedtherectumastheprimarysite.Grosslythemasswasgrey-whiteandcrisptexture.Microscopicexaminationfeaturedreticular,microcystic,macrocystic,papillary,solid,andsomeglandularpatterns.Immunohistochemically,tumorcellsofbothcaseswerepositiveforSALL4,AFP,pan-cytokeratin(AE1/AE3),andglypican-3.Simultaneously,astainforEMA,OCT4,CD30,HCG,vimentinandCK20werenegativeinall2neoplasms.Thefeaturesofmorphology,immunohistochemistry,laboratoryexaminationsandimagingstudiesconsistofthediagnosisofprimaryyolksactumoroftheintestine.